Multivisceral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, Padua, Italy.
Hemorrhagic and Thrombotic Diseases Unit, Department of Medicine (DIMED), University of Padua Medical School, Padua, Italy.
Thromb Haemost. 2020 Aug;120(8):1173-1181. doi: 10.1055/s-0040-1713169. Epub 2020 Jun 30.
Portal vein thrombosis (PVT) is the most common thrombotic complication in cirrhosis; however, local risk factors involved in its pathogenesis are still not fully investigated. The aim of the study was to evaluate hemostasis and endothelial damage in the portal vein in patients with cirrhosis and portal hypertension.
Adult cirrhotics undergoing transjugular intrahepatic portosystemic shunt were consecutively enrolled. Rotational thromboelastometry (ROTEM), dosage of total circulating glycosaminoglycans (GAGs), and endotoxemia levels (lipopolysaccharide [LPS]), along with evaluation of endothelial dysfunction by quantification of circulating endothelial microparticles (MPs), were performed on citrated peripheric and portal venous blood samples from each enrolled patient.
Forty-five cirrhotics were enrolled. ROTEM analysis revealed the presence of a significant heparin-like effect in portal blood (median ɑ angle NATEM 50° vs. HEPTEM 55°, = 0.027; median coagulation time NATEM 665 s vs. HEPTEM 585 s, = 0.006), which was not detected in peripheral blood, and was associated with a higher concentration of circulating GAGs. Even though total annexin V-MP circulating MPs were less concentrated in the splanchnic district, the proportion of MPs of endothelial origin, with respect to annexin V-MP, was significantly increased in the portal district ( = 0.036). LPS concentration was higher in portal (197 pg/mL) compared with peripheral blood (165 pg/mL) ( < 0.001).
Evidences of a damage of glycocalyx along with increased concentration of endothelial MPs suggest the presence of a significant endothelial alteration in the portal vein with respect to peripheral veins. Portal site-specific endothelial damage could hamper its antithrombotic properties and may represent an important local risk factor in the pathogenesis of PVT.
门静脉血栓形成（PVT）是肝硬化最常见的血栓并发症；然而，其发病机制中涉及的局部危险因素仍未得到充分研究。本研究旨在评估肝硬化门静脉高压患者门静脉中的止血和内皮损伤。
连续纳入接受经颈静脉肝内门体分流术的成年肝硬化患者。对每位入组患者的外周和门静脉枸橼酸盐血样进行旋转血栓弹性测定（ROTEM）、总循环糖胺聚糖（GAG）测定和内毒素血症水平（脂多糖[LPS]），并通过定量检测循环内皮微粒（MPs）评估内皮功能障碍。
纳入 45 例肝硬化患者。ROTEM 分析显示门静脉血中存在明显的肝素样效应（中位 NATEM ɑ角 50° vs. HEPTEM 55°， = 0.027；中位 NATEM 凝血时间 665 s vs. HEPTEM 585 s， = 0.006），而在外周血中则未检测到这种效应，且与循环 GAG 浓度较高相关。尽管内脏区总 annexin V-MP 循环 MPs 的浓度较低，但与 annexin V-MP 相比，内皮来源的 MPs 比例在门静脉区显著增加（ = 0.036）。门静脉（197 pg/mL）中的 LPS 浓度高于外周血（165 pg/mL）（ < 0.001）。
糖萼损伤的证据以及内皮 MPs 浓度的增加表明，门静脉相对于外周静脉存在明显的内皮改变。门静脉部位特异性的内皮损伤可能会损害其抗血栓特性，并可能成为 PVT 发病机制中的一个重要局部危险因素。
